ArticleAmerican journal of physiology. Cell physiology2010
Cystic fibrosis transmembrane conductance regulator is involved in airway epithelial wound repair.
Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 83 citations in OpenAlex.
- CFTR ion transport deficiency primes the epithelium for partial epithelial-mesenchymal transition in cystic fibrosis.Frontiers in pharmacology · 2025Article
- Elexacaftor/Tezacaftor/Ivacaftor Accelerates Wound Repair in Cystic Fibrosis Airway Epithelium.Journal of personalized medicine · 2022Article
- Human Amniotic Mesenchymal Stem Cells and Fibroblasts Accelerate Wound Repair of Cystic Fibrosis Epithelium.Life (Basel, Switzerland) · 2022Article
- Targeting the EGFR-ERK axis using the compatible solute ectoine to stabilize CFTR mutant F508del.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Expanding the spectrum of epidermolysis bullosa simplex: Syndromic epidermolysis bullosa simplex with nephropathy and epilepsy secondary to CD151 tetraspanin defect-a case report and review of the literature.JAAD case reports · 2022Article
- CFTR, Cell Junctions and the Cytoskeleton.International journal of molecular sciences · 2022Review
- The Effect of Dynasore Upon the Negative Interaction Between ENaC and CFTR Channels in Xenopus laevis Oocytes.The Journal of membrane biology · 2022Article
- SLC6A14 Impacts Cystic Fibrosis Lung Disease SeverityFrontiers in molecular biosciences · 2022Article
- Esc peptides as novel potentiators of defective cystic fibrosis transmembrane conductance regulator: an unprecedented property of antimicrobial peptides.Cellular and molecular life sciences : CMLS · 2021Article
- Pathophysiology of Lung Disease and Wound Repair in Cystic Fibrosis.Pathophysiology : the official journal of the International Society for Pathophysiology · 2021Review
- Mutant CFTR Drives TWIST1 mediated epithelial-mesenchymal transition.Cell death & disease · 2020Article
- What Role Does CFTR Play in Development, Differentiation, Regeneration and Cancer?International journal of molecular sciences · 2020Review
- The Role of Specialized Pro-Resolving Mediators in Cystic Fibrosis Airways Disease.Frontiers in pharmacology · 2020Review
- Deletion ofFrontiers in immunology · 2020Article
- Bronchial epithelium repair by Esculentin-1a-derived antimicrobial peptides: involvement of metalloproteinase-9 and interleukin-8, and evaluation of peptides' immunogenicity.Scientific reports · 2019Article
- Transcriptomic profile of cystic fibrosis airway epithelial cells undergoing repair.Scientific data · 2019Article
- Repair Process Impairment byFrontiers in cellular and infection microbiology · 2019Review
- Airway Epithelium Dysfunction in Cystic Fibrosis and COPD.Mediators of inflammation · 2018Review
- Linear array of multi-substrate tracts for simultaneous assessment of cell adhesion, migration, and differentiation.BioTechniques · 2017Article
- MicroRNA-9 downregulates the ANO1 chloride channel and contributes to cystic fibrosis lung pathology.Nature communications · 2017Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
The role of cystic fibrosis (CF) transmembrane conductance regulator (CFTR) in airway epithelial wound repair was investigated using normal human bronchial epithelial (NHBE) cells and a human airway epithelial cell line (Calu-3) of serous gland origin. Measurements of wound repair were performed using continuous impedance sensing to determine the time course for wound closure. Control experiments showed that the increase in impedance corresponding to cell migration into the wound was blocked by treatment with the actin polymerization inhibitor, cytochalasin D. Time lapse imaging revealed that NHBE and Calu-3 cell wound closure was dependent on cell migration, and that movement occurred as a collective sheet of cells. Selective inhibition of CFTR activity with CFTR(inh)-172 or short hairpin RNA silencing of CFTR expression produced a significant delay in wound repair. The CF cell line UNCCF1T also exhibited significantly slower migration than comparable normal airway epithelial cells. Inhibition of CFTR-dependent anion transport by treatment with CFTR(inh)-172 slowed wound closure to the same extent as silencing CFTR protein expression, indicating that ion transport by CFTR plays a critical role in migration. Moreover, morphologic analysis of migrating cells revealed that CFTR inhibition or silencing significantly reduced lamellipodia protrusion. These findings support the conclusion that CFTR participates in airway epithelial wound repair by a mechanism involving anion transport that is coupled to the regulation of lamellipodia protrusion at the leading edge of the cell.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.